- |||||||||| limantrafin (CB-103) / Cellestia Biotech, Lenvima (lenvatinib) / Eisai, Merck (MSD), Verzenio (abemaciclib) / Eli Lilly
Enrollment closed, Enrollment change: CB-103 With Either Lenvatinib or Abemaciclib in Patients With NOTCH ACC (clinicaltrials.gov) - Oct 1, 2024
P1/2, N=10, Active, not recruiting,
To proceed with clinical translation of these treatments, we need additional research to fully explain the activities of the three agents toward expression of cancer stem cell markers on PANC-1 and other PDAC cell line spheroids. Recruiting --> Active, not recruiting | N=34 --> 10
- |||||||||| Venclexta (venetoclax) / Roche, AbbVie, limantrafin (CB-103) / Cellestia Biotech
Enrollment change, Trial completion date, Trial termination, Trial primary completion date: Phase II Study to Evaluate Safety and Efficacy of CB-103 With Venetoclax in Adolescent and Young Adult Patients With Relapsed/Refractory T-ALL or T-LBL (clinicaltrials.gov) - Aug 19, 2024
P2, N=2, Terminated,
Recruiting --> Active, not recruiting | N=34 --> 10 N=30 --> 2 | Trial completion date: Jul 2026 --> Aug 2024 | Recruiting --> Terminated | Trial primary completion date: Jul 2026 --> Aug 2024; The sponsor requested termination due to internal reprioritization of resources.
- |||||||||| limantrafin (CB-103) / Cellestia Biotech, Lenvima (lenvatinib) / Eisai, Merck (MSD), Verzenio (abemaciclib) / Eli Lilly
Trial primary completion date: CB-103 With Either Lenvatinib or Abemaciclib in Patients With NOTCH ACC (clinicaltrials.gov) - Jun 16, 2024
P1/2, N=34, Recruiting,
However, further studies on the mechanism of action of AMPs in keratinocytes and clinical trials are needed. Trial primary completion date: Jun 2024 --> Jun 2025
- |||||||||| limantrafin (CB-103) / Cellestia Biotech
Enrollment change, Trial termination: CAILA: CB-103 Plus NSAI In Luminal Advanced Breast Cancer (clinicaltrials.gov) - Dec 19, 2023
P2, N=2, Terminated,
We propose the revised and updated E locus dominance hierarchy to be E ?>?E?>?e /e /e ?>?e . N=80 --> 2 | Active, not recruiting --> Terminated; Sponsor decision
- |||||||||| CB-103 / Cellestia Biotech
Journal: Evaluation of the anticancer activity of RIN-1, a Notch signaling modulator, in head and neck squamous cell carcinoma. (Pubmed Central) - Aug 22, 2023
Here, we present the growth- and differentiation-modulating effects of various "next generation" small molecule Notch modulators represented by RIN-1, and CB-103, on HNSCC, compared to gamma secretase inhibitors as "conventional" NOTCH interfering compounds, like DAPT...In contrast, RIN-1 treatment resulted in inhibition of Notch signalling and the growth of HNSCC spheroids under non-adherent cell culture conditions. Our results suggest that modulation of Notch signalling could be used as a chemotherapeutic agent in selected patients with intact NOTCH signaling.
- |||||||||| CB-103 / Cellestia Biotech
Preclinical, Journal: The Efficacy of CB-103, a First-in-Class Transcriptional Notch Inhibitor, in Preclinical Models of Breast Cancer. (Pubmed Central) - Aug 12, 2023
Our results suggest that modulation of Notch signalling could be used as a chemotherapeutic agent in selected patients with intact NOTCH signaling. our data indicate that CB-103 is an attractive candidate for clinical investigation in endocrine-resistant, recurrent breast cancers with biomarker-confirmed Notch activity in combination with SERDs and/or CDKis and in TNBCs with biomarker-confirmed Notch activity in combination with taxane-containing chemotherapy regimens.
- |||||||||| CB-103 / Cellestia Biotech
Journal, IO biomarker: Effect of Allergen-Specific Immunotherapy on Transcriptomic Changes in Canine Atopic Dermatitis. (Pubmed Central) - Aug 2, 2023
Based on the available literature, we chose nine differentially expressed genes (RARRES2, DPP10, SLPI, PLSCR4, MMP9, NTSR1, CBD103, DEFB122, and IL36G) which may be important in the context of the dysregulated immune response observed in cAD patients...The expressions of three of these genes returned to the level observed in the healthy control group. The genes listed above need further investigation to determine details of their role in the molecular mechanism of immune tolerance induction in response to allergen-specific immunotherapy.
- |||||||||| limantrafin (CB-103) / Cellestia Biotech, Lenvima (lenvatinib) / Eisai, Merck (MSD), Verzenio (abemaciclib) / Eli Lilly
Enrollment open: CB-103 With Either Lenvatinib or Abemaciclib in Patients With NOTCH ACC (clinicaltrials.gov) - Jun 5, 2023
P1/2, N=34, Recruiting,
The genes listed above need further investigation to determine details of their role in the molecular mechanism of immune tolerance induction in response to allergen-specific immunotherapy. Not yet recruiting --> Recruiting
- |||||||||| limantrafin (CB-103) / Cellestia Biotech
Trial completion date, Trial primary completion date: Study of CB-103 in Adult Patients With Advanced or Metastatic Solid Tumours and Haematological Malignancies (clinicaltrials.gov) - Jan 21, 2022
P1/2, N=200, Recruiting,
Preliminary pre-clinical and clinical data shows desirable safety and efficacy profile of CB-103 enabling clinical development in combination with several therapeutic agents. Trial completion date: Dec 2021 --> Dec 2022 | Trial primary completion date: Dec 2021 --> Oct 2022
- |||||||||| limantrafin (CB-103) / Cellestia Biotech
Enrollment closed: CAILA: CB-103 Plus NSAI In Luminal Advanced Breast Cancer (clinicaltrials.gov) - Oct 26, 2021
P2, N=80, Active, not recruiting,
These results open the possibility for studies testing VitD as an adjuvant in leishmaniasis therapy. Recruiting --> Active, not recruiting
- |||||||||| nirogacestat (PF-03084014) / SpringWorks Therap
Journal: Targeting pathogenic mechanisms in marginal zone lymphoma: from concepts and beyond. (Pubmed Central) - Oct 22, 2021
NOTCH signaling is also crucial for marginal zone cells, but no clinical data are available with NOTCH inhibitors such as the γ-secretase inhibitor PF-03084014 or the NICD inhibitor CB-103. The hypermethylation phenotype, the overexpression of the PRC2-complex or the presence of TET2 mutations reported in MZL subsets make epigenetic agents (demethylating agents, EZH2 inhibitors, HDAC inhibitors) also potential therapeutic tools for MZL patients.
- |||||||||| CB-103 / Cellestia Biotech
[VIRTUAL] Cellestia Biotech AG () - May 31, 2021 - Abstract #BIO2021BIO_289;
Further, Cellestia is advancing a rich R&D pipeline of novel transcription factor inhibitors, in oncology, auto-immune and inflammatory disorders, having achieved animal in-vivo proof of concept for several new targets. Cellestia was founded in 2014 as a spin-off from EPFL, Lausanne, Switzerland and is headquartered in Basel, Switzerland
- |||||||||| limantrafin (CB-103) / Cellestia Biotech
Enrollment open, Trial initiation date: CAILA: CB-103 Plus NSAI In Luminal Advanced Breast Cancer (clinicaltrials.gov) - Apr 20, 2021
P2, N=80, Recruiting,
The RP2D has been established for advancing clinical development into phase 2. Not yet recruiting --> Recruiting | Initiation date: Jan 2021 --> Apr 2021
- |||||||||| CB-103 / Cellestia Biotech
Journal: Notch Inhibition in Cancer: Challenges and Opportunities. (Pubmed Central) - Nov 1, 2020
Our lead molecule, CB-103 is currently being investigated in Phase-1 dose escalation in cancer patients. Cellestia Biothech is further expanding its medicinal chemistry activities advancing the development of novel molecules for targeting transcription factors in cancer as well as non-cancer indications.
- |||||||||| limantrafin (CB-103) / Cellestia Biotech
Trial completion date, Trial primary completion date: Study of CB-103 in Adult Patients With Advanced or Metastatic Solid Tumours and Haematological Malignancies (clinicaltrials.gov) - Oct 7, 2020
P1/2, N=165, Recruiting,
Cellestia Biothech is further expanding its medicinal chemistry activities advancing the development of novel molecules for targeting transcription factors in cancer as well as non-cancer indications. Trial completion date: Jun 2021 --> Dec 2021 | Trial primary completion date: Jun 2021 --> Dec 2021
- |||||||||| CB-103 / Cellestia Biotech
Journal: Pharmacological disruption of the Notch transcription factor complex. (Pubmed Central) - Sep 25, 2020
CB-103 produces Notch loss-of-function phenotypes in flies and mice and inhibits the growth of human breast cancer and leukemia xenografts, notably without causing the dose-limiting intestinal toxicity associated with other Notch inhibitors. Thus, we describe a pharmacological strategy that interferes with Notch signaling by disrupting the Notch transcription complex and shows therapeutic potential for treating Notch-driven cancers.
- |||||||||| CB-103 / Cellestia Biotech
Journal: Activity and transcriptional regulatory elements of the promoter in Arctic fox (Vulpes lagopus) β-defensin103 gene (Pubmed Central) - Sep 12, 2019
The region of -1 604 /+51 was the core promoter region of CBD103 gene in Arctic fox and -1 552/-1 564, -1 439/-1 454 and -329/-339 regions were positive regulatory regions. This study successfully obtained the core promoter region and positive regulation regions of the Arctic fox CBD103 gene, which laid a foundation for further study on the molecular genetic mechanism of this gene regulating Arctic fox coat color.
- |||||||||| CB-103 / Cellestia Biotech
Journal: Duodenal expression of antimicrobial peptides in dogs with idiopathic inflammatory bowel disease and intestinal lymphoma. (Pubmed Central) - Aug 27, 2019
...Duodenal mRNA expression of six representative AMPs - lactoferrin, lysozyme, cathelicidin, secretory leukocyte peptidase inhibitor (SLPI), bactericidal/permeability increasing protein (BPI), and canine beta defensin (CBD103) - was quantified by real-time reverse transcription polymerase chain reaction...Increased expression of BPI differentiated IBD from dogs with small cell intestinal lymphoma, with a sensitivity of 93.2%, a specificity of 100%, and an area under the curve of 0.955. These results suggest that the expression patterns of AMP aid in the diagnosis of canine IBD and intestinal lymphoma, although it remains uncertain whether the altered AMP expression is the cause or effect of mucosal inflammation.
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